Sphingosine kinase 1 enhances the invasion and migration of non-small cell lung cancer cells via the AKT pathway

被引:30
|
作者
Zhu, Liangming [1 ]
Wang, Zhou [2 ]
Lin, Yuxia [1 ]
Chen, Zhitao [1 ]
Liu, Haibo [1 ]
Chen, Ying [1 ]
Wang, Ningning [3 ]
Song, Xiue [3 ]
机构
[1] Shandong Univ, Dept Thorac Surg, Jinan Cent Hosp, Jinan 250013, Shandong, Peoples R China
[2] Shandong Univ, Dept Thorac Surg, Shandong Prov Hosp, Jinan 250013, Shandong, Peoples R China
[3] Shandong Univ, Dept Obstet & Gynaecol, Jinan Cent Hosp, Jinan 250013, Shandong, Peoples R China
关键词
SphK1; invasion; migration; non-small cell lung cancer; EMT; AKT; COLON-CANCER; PROGRESSION; PROLIFERATION; EXPRESSION; SURVIVAL; GROWTH; SPHK1; SPHINGOSINE-1-PHOSPHATE; METASTASIS; APOPTOSIS;
D O I
10.3892/or.2014.3683
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Sphingosine kinase 1 (SphK1) has been shown to play an important role in the progression of a number of human cancers. It has been reported that the expression of SphK1 is greatly elevated in non-small cell lung cancer (NSCLC) tissues. However, its role and underlying mechanisms in NSCLC have not been fully elucidated. In the present study, we found that SphK1 was highly expressed in NSCLC cells. Overexpression of SphK1 promoted the invasion and migration of NSCLC cells, while knockdown of SphK1 suppressed the invasion and migration. Furthermore, we demonstrated that SphK1 decreased the protein level of E-cadherin, yet increased the protein level of Snail. In addition, SphK1 was able to stimulate the activation of AKT. Inhibition of the AKT pathway attenuated the biological functions of NSCLC cells induced by overexpression of SphK1. Taken together, our findings suggest that SphK1 can enhance the invasion and migration of NSCLC cells via activation of the AKT pathway and regulation of E-cadherin and Snail expression. Thus, SphK1 could be a potential target for the detection and treatment of NSCLC.
引用
收藏
页码:1257 / 1263
页数:7
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